Evidence map›Paper›PMID 38652539›Full record

ArticleJCI insight2024

miRNA-148a-containing GMSC-derived EVs modulate Treg/Th17 balance via IKKB/NF-κB pathway and treat a rheumatoid arthritis model.

Jingrong Chen, Xiaoyi Shi, Yanan Deng, Junlong Dang, Yan Liu, Jun Zhao, Rongzhen Liang, Donglan Zeng, Wenbin Wu, Yiding Xiong and 10 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in JCI insight, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
8.7field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

20 authors at 7 institutions in 2 countries.

Jingrong ChenDepartment of Immunology, School of Cell and Gene Therapy, Shanghai Songjiang Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Xiaoyi ShiDepartment of Internal Medicine, Division of Rheumatology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Yanan DengDepartment of Immunology, School of Cell and Gene Therapy, Shanghai Songjiang Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Junlong DangDepartment of Immunology, School of Cell and Gene Therapy, Shanghai Songjiang Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yan LiuDepartment of Internal Medicine, Division of Rheumatology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Jun ZhaoDepartment of Immunology, School of Cell and Gene Therapy, Shanghai Songjiang Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Rongzhen LiangDepartment of Immunology, School of Cell and Gene Therapy, Shanghai Songjiang Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Donglan ZengDepartment of Clinical Immunology.
Wenbin WuDepartment of Spine Surgery, and.
Yiding XiongDepartment of Immunology, School of Cell and Gene Therapy, Shanghai Songjiang Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Jia YuanDepartment of Stomatology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Ye ChenDepartment of Immunology, School of Cell and Gene Therapy, Shanghai Songjiang Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Julie WangDepartment of Immunology, School of Cell and Gene Therapy, Shanghai Songjiang Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Weidong LinDepartment of Immunology, School of Cell and Gene Therapy, Shanghai Songjiang Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Xiangfang ChenDepartment of Endocrinology, Second Affiliated Hospital of Naval Medical University, Shanghai, China.
Weishan HuangDepartment of Pathobiological Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, Louisiana, USA.
Nancy OlsenDivision of Rheumatology, Department of Medicine, The Penn State University Hershey Medical Center, Hershey, Pennsylvania, USA.
Yunfeng PanDepartment of Internal Medicine, Division of Rheumatology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Qingling FuOtorhinolaryngology Hospital, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Song Guo ZhengDepartment of Immunology, School of Cell and Gene Therapy, Shanghai Songjiang Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Shanghai Jiao Tong University · CNThird Affiliated Hospital of Sun Yat-sen University · CNSun Yat-sen University · CNLouisiana State University · USPenn State Milton S. Hershey Medical Center · USShanghai Changzheng Hospital · CNThe First Affiliated Hospital, Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mesenchymal stem cells (MSCs) have demonstrated potent immunomodulatory properties that have shown promise in the treatment of autoimmune diseases, including rheumatoid arthritis (RA). However, the inherent heterogeneity of MSCs triggered conflicting therapeutic outcomes, raising safety concerns and limiting their clinical application. This study aimed to investigate the potential of extracellular vesicles derived from human gingival mesenchymal stem cells (GMSC-EVs) as a therapeutic strategy for RA. Through in vivo experiments using an experimental RA model, our results demonstrate that GMSC-EVs selectively homed to inflamed joints and recovered Treg and Th17 cell balance, resulting in the reduction of arthritis progression. Our investigations also uncovered miR-148a-3p as a critical contributor to the Treg/Th17 balance modulation via IKKB/NF-κB signaling orchestrated by GMSC-EVs, which was subsequently validated in a model of human xenograft versus host disease (xGvHD). Furthermore, we successfully developed a humanized animal model by utilizing synovial fibroblasts obtained from patients with RA (RASFs). We found that GMSC-EVs impeded the invasiveness of RASFs and minimized cartilage destruction, indicating their potential therapeutic efficacy in the context of patients with RA. Overall, the unique characteristics - including reduced immunogenicity, simplified administration, and inherent ability to target inflamed tissues - position GMSC-EVs as a viable alternative for RA and other autoimmune diseases.

Indexed as

Arthritis, RheumatoidExtracellular VesiclesMesenchymal Stem CellsMicroRNAsSignal TransductionTh17 CellsT-Lymphocytes, RegulatoryAnimalsDisease Models, AnimalFibroblastsGingivaHumansI-kappa B KinaseMaleMiceNF-kappa BI-kappa B KinaseMicroRNAsMIRN148 microRNA, humanNF-kappa BAutoimmune diseasesAutoimmunityStem cellsStem cell transplantation

Identifiers

PMID38652539
PMCPMC11141912
OpenAlexW4395050561

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.